Distinct structural and molecular features of the myocardial extracellular matrix remodeling in compensated and decompensated cardiac hypertrophy due to aortic stenosis

Polyakova, V. O.; Richter, Manfred; Ganceva, Natalia; Lautze, Hans-Jürgen; Kamata, Satoshi; Pöling, Jochen; Beiras-Fernández, Andrés; Hein, Stefan; Szalay, Z.; Braun, Thomas; Walther, Thomas; Kostin, Sawa

doi:10.1016/j.ijchv.2014.05.001

Cited by 5 publications

(4 citation statements)

References 70 publications

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“…MF results from disruption of the equilibrium between the synthesis and degradation of collagen, which leads to an excessive accumulation of collagen fibers in the myocardium [2]. The pathogenesis of MF is not completely clear; its regulation involves the extracellular matrix (ECM) system [3], the renin-angiotensin aldosterone system [4,5], a variety of cytokines, cell apoptosis and other systems [6]. …”

Section: Introductionmentioning

confidence: 99%

Prenatal Exposure to Lipopolysaccharide Results in Myocardial Fibrosis in Rat Offspring

Chen

Tang

Gao

et al. 2015

IJMS

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The epigenetic plasticity hypothesis indicates that exposure during pregnancy may cause adult-onset disorders, including hypertension, myocardial infarction and heart failure. Moreover, myocardial fibrosis coincides with hypertension, myocardial infarction and heart failure. This study was designed to investigate the effects of prenatal exposure to lipopolysaccharide (LPS) on myocardial fibrosis. The result showed that at six and 16 weeks of age, the LPS-treated offspring exhibited increased collagen synthesis, an elevated cardiac index (CI), higher mRNA levels of TIMP-2 and TGFβ and a reduced mRNA level of MMP2. The protein levels corresponded to the mRNA levels. The offspring that were prenatally treated with pyrrolidine dithiocarbamic acid (PDTC), an inhibitor of NF-κB, displayed improvements in the CI and in collagen synthesis. Moreover, PDTC ameliorated the expression of cytokines and proteins associated with myocardial fibrosis. The results showed that maternal inflammation can induce myocardial fibrosis in offspring during aging accompanied by an imbalance of TIMP-2/MMP2 and TGFβ expression.

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Section: Introductionmentioning

confidence: 99%

Prenatal Exposure to Lipopolysaccharide Results in Myocardial Fibrosis in Rat Offspring

Chen

Tang

Gao

et al. 2015

IJMS

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“…Adaptation of cardiac hypertrophy by the induction of a genetic program leads to increased protein synthesis and increased size of cardiomyocytes [3]. LVH is accompanied by loss of cardiomyocytes, reorganization of extracellular matrix (ECM), and increased ECM elements [4]. During progression of hypertrophy, the expression profile of numerous genes changes, which ultimately results in impairments in the performance of the heart [5].…”

Section: Introductionmentioning

confidence: 99%

The effect of resveratrol on angiotensin II levels and the rate of transcription of its receptors in the rat cardiac hypertrophy model

et al. 2016

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This study investigated the effect of resveratrol on serum and cardiac levels of angiotensin II and transcription of its main receptors following pressure overload induced-hypertrophy. Rats were divided into untreated (Hyp) and resveratrol treated hypertrophied groups (H + R). Intact animals served as the control (Ctl). Cardiac hypertrophy was induced by abdominal aortic banding. Blood pressure (BP) was recorded via left carotid artery cannula. Fibrosis was confirmed by Masson trichrome staining. Angiotensin II level was measured using an ELIZA test. Gene expression was assessed by a real time PCR (RT-PCR) technique. We observed that in the H + R group BP and heart weight/body weight were decreased significantly (p < 0.001, p < 0.05, respectively vs Hyp). The cardiac levels of angiotensin II and AT1a mRNA were increased in the Hyp group (p < 0.01 vs Ctl). In the H + R group the AT1a mRNA level was decreased significantly (p < 0.05 vs Hyp). It could be concluded that resveratrol protects the heart against hypertrophy progression in part by affecting cardiac AT1a transcription.

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“…Recently it has been demonstrated that deletion of collagen V in mice has a protective effect after myocardial infarction by reducing fibrosis and pathological remodelling [16] . Our previous study has shown that expression levels of collagen V clearly distinguishes compensated from decompensated left ventricular hypertrophy in patients with aortic stenosis [7] . Therefore, in the present study we hypothesized that collagen V may play a role in the development of atrial fibrosis thereby contributing to the maintenance of AF in humans.…”

Section: Introductionmentioning

confidence: 92%

“…The major heart collagens are collagen type I and type III that comprise almost 95 % of the [7] extracellular matrix [8] , [9] . Although these collagens are the most prevalent in cardiac tissue and their role in myocardial remodelling is increasingly studied, the role of the minor fibrillar collagens such as collagen type V is less studied.…”

Section: Introductionmentioning

confidence: 99%

Atrial fibrillation in human patients is associated with increased collagen type V and TGFbeta1

Kostin,

Richter,

Ganceva

et al. 2024

IJC Heart & Vasculature

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Distinct structural and molecular features of the myocardial extracellular matrix remodeling in compensated and decompensated cardiac hypertrophy due to aortic stenosis

Cited by 5 publications

References 70 publications

Prenatal Exposure to Lipopolysaccharide Results in Myocardial Fibrosis in Rat Offspring

Prenatal Exposure to Lipopolysaccharide Results in Myocardial Fibrosis in Rat Offspring

The effect of resveratrol on angiotensin II levels and the rate of transcription of its receptors in the rat cardiac hypertrophy model

Atrial fibrillation in human patients is associated with increased collagen type V and TGFbeta1

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